CHLOROTHALONIL MAKES A COMEBACK

One of the main talking points this month in Europe in the agricultural press has been the rapid onset of resistance in Septoria tritici (recently renamed by the taxonomists as Mycosphaerella graminicola) to strobilurin fungicides and how to manage the consequences effectively in this year’s wheat crops. Since their first introduction in Germany in 1996, strobilurin fungicides have come to dominate cereal disease control with the added bonus of a distinctive “greening effect” which enhances yields. There had already been significant incidences of resistance in powdery mildew in Germany but this latest issue has prompted a closer look at the causes.

Professor Ulrich Gisi of Syngenta AG is a global expert on resistance based at the company’s research centre in Stein, Switzerland. According to his figures, the occurrence of Mycosphaerella graminicola resistance to strobilurin fungicides increased from 31% of samples taken in England in 2002 to 71% in 2003 (and to as high as 87% by other estimates) and from 17% to 43% in Scotland.

This sudden increase in resistance is related to the mode of action of the “QoI” fungicides, which include the strobilurins as well as famoxadone and fenamidone. These fungicides stop electron flow and energy utilisation in plant mitochondria by binding at a very specific location on the “Qo respiration site”, namely the glutamic acid at amino acid position 272. This site-specific activity presents a high risk of resistance. A major mechanism of resistance has been a change in the closely situated amino acid at position 143. This is normally glycine, but, if it is changed by point mutation to alanine, the QoI fungicide is blocked from binding and resistance occurs. This mutation is naturally present in the forest mushrooms in which strobilurins were originally discovered.
Resistance to QoI fungicides in powdery mildew is already quite widespread on wheat, but on barley it has not evolved so quickly. Resistance in cereal rusts, Rhynchosporium and Pyrenophora has not been detected so far. There were no signs of resistance to Mycosphaerella graminicola in Europe until 2001, when very low levels were detected. Syngenta’s own research in 2002 in the UK, Ireland, France, Belgium and Germany detected about 5% of isolates with resistance in bioassay and molecular tests. This figure rose rapidly and in pre-season monitoring in May 2003 Syngenta found that about a third of Mycosphaerella isolates showed resistance. All samples taken showed evidence of resistance but there was a huge variation in the populations, from 6-93%. There was a particularly high incidence in Ireland. The proportion of resistance found in the 2003 samples increased very significantly after fungicide treatment, causing considerable concern.

Sensitivity shifts with triazoles

Resistance of Mycosphaerella graminicola to DMI fungicides such as the triazoles has evolved slowly in Europe since 1989. These compounds inhibit a demethylation step in sterol biosynthesis and the development of resistance to them is a more complex process than with strobilurins, according to Dr Gisi. There are at least three mechanisms that can be involved and the level of resistance that develops is not so high.
However, there has been a gradual shift in sensitivity to these fungicides from 1991 to 2003, by a factor of about four according to Syngenta, with little differences between individual triazoles. Use of reduced rates of triazoles has also apparently promoted selection of the less sensitive parts of the population, although this is not the case with QoIs. In practice, this means that 4-7 times the dose rates of triazoles originally used are now required to give comparable levels of control to those originally achieved.